Both adhesion and cell signaling molecules have been shown to play a role in the morphological and functional changes involved in synaptic plasticity in Aplysia, rats and chicks, and most recently, Drosophila. Changes in synaptic architecture can be triggered by stimuli that promote learning, and mutations in adhesion molecules can affect both synaptic plasticity and the processes of learning and memory. In particular, integrins are adhesion molecules that also function in signal transduction that have an expression pattern and mutant phenotype in the nervous system suggestive of a role in synaptic plasticity. As well, mutations in one Drosophila integrin, the alpha subunit encoded by the Volado gene, have been shown to affect both olfactory learning and function at the NMJ. Integrin agonists have also been shown to disrupt the stabilization of LTP in hippocampal slice preparations. The Drosophila neuromuscular junction is an excellent model system for incorporating genetic, molecular and cellular techniques in the study of the role of integrins in morphology and function at the synapse and thereby in synaptic plasticity, learning and memory.